Lipoinfiltración de gran volumen en un caso de lipodistrofia glútea profunda / Lipofilling of large volume in a case of deep gluteal lipodistrophy

La lipoinyección de grasa autóloga es una técnica habitual en Cirugía Estética. Los refinamientos en los procesos de extracción, preparación y reintroducción de la grasa han permitido una mayor supervivencia ylos buenos resultados obtenidos han contribuido a extender las indicaciones de la lipoinfiltración al terreno de la Cirugía Reconstructiva y a defectos mayores. Presentamos un caso de lipodistrofia glútea profunda, secundaria a una vacuna, que se trató mediante trasplante de 300cc de grasa autóloga. Se describen los detalles técnicos y las ventajas de este procedimiento frente a otras alternativas terapeúticas. El resultado inicial mejoró durante 6 meses y fue muy satisfactorio para la paciente y los cirujanos. Pensamos que este es otro caso que apoya la “teoría de la supervivencia” de adipocitos y adipoblastos (AU)

Lipofilling is a common technnique in Aesthetic Surgery. Refinements in the process of extraction, preparation and reintroduction of the fat have allowed an increased survival and the excellent obtained results have contributed to extend the indications of lipoinfiltration to the field of Reconstructive Surgery and therefore to cover larger defects. We present a case of deep gluteal lipodistrophy, secondary to vaccination, was treated with a 300 autologous fat transplant. We describe technical details and advantages of this procedure versus other therapeutic options. The initial result improved over 6 months and was very satisfactory for the patient and the surgeons. We believe this is another case that supports the “survival theory” of adipocytes and adipoblasts (AU)

Castration restores function and neurofilament alterations of aged symptomatic males in a transgenic mouse model of spinal and bulbar muscular atrophy.

Transgenic models of neurodegenerative disease have proved uniquely powerful for delineating pathways of neuronal dysfunction and cell death. We have developed a transgenic model of the polyglutamine disease spinal and bulbar muscular atrophy (SBMA), an adult-onset, slowly progressive motor neuron disease caused by polyglutamine expansion in the androgen receptor (AR). Mice bearing a human AR with 112 glutamines reproduce many aspects of SBMA, including slowly progressive, gender-specific motor deficits, and neuronal intranuclear inclusions. Despite substantial motor deficits in male AR112Q mice, no motor neuron loss was observed, indicating that neuronal dysfunction, rather than neuronal death, is central to disease. Moreover, reduced levels of unphosphorylated neurofilament heavy chain (NF-H) were observed in motor neurons, suggesting a role for NF-H in SBMA neuronal dysfunction. The elimination of androgens by surgical castration of severely affected, aged 112Q male mice partially restored motor function as well as NF-H levels. These data suggest that hormone-based therapies designed to treat SBMA patients, even with advanced disease, are likely to be effective.